Talk to us?

- NEETMDS- courses
NEET MDS Lessons
General Pathology

G-6 PD Deficiency

Occurs in Negroes, Mediterranean races, India and far East. It confers a protection Against falciparum malaria.

It is transmitted as X-linked trait of intermediate dominance (variable effect in homozygous females). 

Haemolysis may be induced by :
•    Primaquin and other anti malarials.
•    Other drugs like chloramphenicol , analgesics, antitubercular drugs etc.
•    Infections.
•    Ingestion of Vicia faba bean (favism).
•    Diabetic acidosis
 

OEDEMA

 Excessive accumulation of fluid in the extra vascular compartment (intersttitial tissues). This includes ascites (peritoneal sac), hydrothorax (pleural cavity) hydropericardium (pericardial space) and anasarca (generalised)

Factors which tend to accumulate interstitial fluid are:

- Intravascular hydrostatic pressure

- Interstitial osmotic pressure.

- Defective lymphatic drainage.

- Increased capillary permeability.

Factors that draw fluid into circulation are:

- Tissue hydrostatic-pressure (tissue tension).

- Plasma osmotic pressure,

Oedema fluid can be of 2 types:

A. Exudate.

It is formed due to increased capillary permeability as in inflammation.

B. Transudate

Caused by alterations of hydrostatic and osmotic pressures.

 

Exudate

Transudate

Specific Gravity

>1.018

1.012

Protein Content

High

Low

Nature of Protein

All Plasma Protein

Albumin mostly

Spontaneous Clotting

High(Inflammatory Cells)

Low

Local Oedema

1. Inflammatory oedema. Mechanisms are.

- Increased capillary permeability.

- Increased vascular hydrostatic pressure.

- Increased tissue osmotic pressure.

2.Hypersensitivity reactions especially types I and III

3. Venous obstruction :

- Thrombosis.

- Pressure from outside as in pregnancy, tourniquets.

4. Lymphatic obstruction:

- Elephantiasis in fillariasis

- Malignancies (Peau de orange in breast cancer).

Generalized Oedema

1.         Cardiac oedema

Factors :Venous pressure increased.

2. Renal oedema

- Acute glomerulonephritis

- Nephrotic syndrome

3. Nutritional (hypoproteinaemic) oedema. it is seen in

- Starvation and Kwashiorkor

- Protein losing enteropathy

4.  Hepatic oedema (predominantly ascites)

Factors:

- Fall in plasma protein synthesis

- Raised regional lymphatic and portal venous pressure

5. Oedema due to adrenal corticoids

As in Cushing's Syndrome

Pulmonary oedema

- Left heart failure and mitral stenosis.

- Rapid flv infusion specially in a patient of heart failure.

Nonspecific or Innate Immunity

1. Genetic factors

  • Species: Guinea pig is very susceptible to tuberculosis.
  • Race: Negroes are more susceptible to tuberculosis than whites
  • Sickle cells (HbS-a genetic determined Haemoglobinopathy resistant to Malarial parasite.

2. Age Extremes of age are more susceptible.

3. Hormonal status. Low resistance in:

  • Diabetes Mellitus.
  • Increased corticosteroid levels.
  • Hypothyroidism

4. Phagocytosis. Infections can Occur in :

  • Qualitative  or quantitative defects in neutrophils and monocytes.
  • Diseases of mononuclear phagocytic system (Reticuloendothelial cells-RES).
  • Overload blockade of RES.

5. Humoral factors

  • Lysozyme.
  • Opsonins.
  • Complement
  • Interferon (antiviral agent secreted by cells infected by virus)

Neutropenia: Neutropenia is an abnormally low number of neutrophils  
Causes

-Typhoid, paratyphoid. .
-Viral and ricketseal infections.
-Malaria, Kala azar.
-Hypersplenism.
-Aplastic and megaloblastic anaemia.
-Marrow infiltration by malignancies, lymphomas etc.
-SLE.

Cor pulmonale
a failure of the right side of the heart. It is caused by prolonged high blood pressure in the right ventricle of the heart, which in turn is most often caused by pulmonary hypertension - prolonged high blood pressure in the arteries or veins of the lungs. People with heart disease, or lung diseases such as cystic fibrosis, are at greater risk.

Pathophysiology

There are several mechanisms leading to pulmonary hypertension and cor pulmonale:
Pulmonary vasoconstriction
Anatomic changes in vascularisation
Increased blood viscosity
Primary pulmonary hypertension

Causes

Acute: 
•    Massive pulmonary embolization
•    Exacerbation of chronic cor pulmonale
Chronic: 
•    COPD
•    Loss of lung tissue following trauma or surgery
 

Pulmonary edema

Pulmonary edema is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure.

Signs and symptoms

Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to death, generally due to its main complication of acute respiratory distress syndrome.

Diagnosis

physical examination: end-inspiratory crackles during auscultation (listening to the breathing through a stethoscope) can be due to pulmonary edema. The diagnosis is confirmed on X-ray of the lungs, which shows increased vascular filling and fluid in the alveolar walls.

Low oxygen saturation and disturbed arterial blood gas readings may strengthen the diagnosis

Causes

Cardiogenic causes:

  1. Heart failure
  2. Tachy- or bradyarrhythmias
  3. Severe heart attack
  4. Hypertensive crisis
  5. Excess body fluids, e.g. from kidney failure
  6. Pericardial effusion with tamponade

Non-cardiogenic causes, or ARDS (acute respiratory distress syndrome):

  1. Inhalation of toxic gases
  2. Multiple blood transfusions
  3. Severe infection
  4. Pulmonary contusion, i.e. high-energy trauma
  5. Multitrauma, i.e. severe car accident
  6. Neurogenic, i.e. cerebrovascular accident (CVA)
  7. Aspiration, i.e. gastric fluid or in case of drowning
  8. Certain types of medication
  9. Upper airway obstruction
  10. Reexpansion, i.e. postpneumonectomy or large volume thoracentesis
  11. Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
  12. Lack of proper altitude acclimatization.

Treatment

When circulatory causes have led to pulmonary edema, treatment with loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. Secondly, one can start with noninvasive ventilation. Other useful treatments include glyceryl trinitrate, CPAP and oxygen.

EMBOLISM

Definition: transportation of an abnormal mass of an abnormal mass of undissolved material from one part of circulation to another. The mass transported is called embolus.

Types
I .Thrombi and clots.
2. Gas or air.
3. Fat
4.Amniotic fluid.
5.Tumour

Thromboembolism 
This is the commonest type of embolus and may be formed of the primary thrombus  or more often of propagated clot region which is loosely attached.

Emboli from venous thrombi can result In impaction in the pulmonary  arteries and result in sudden death.
Embolism from cardiac or arterial thrombi results in systemic embolism causing infraction and gangrene.

Gaseous
This occurs when gas is introduced into the circulation:
•    Accidental opening of large veins during surgery.
•    Mismanaged transfusion. .
As air is  readily absorbed into blood only  sudden introduction or large quantities of air produces effects
Caisson’s Disease  bubbling of nitrogen from the blood during sudden decompression as seen during deep sea diving.

Fat Embolism
Causes
•    Fractures especially of long bones and multiple
•    Crush injuries.

Sites of impaction:

o    Lungs.
o    Systemic: causing -
    →    petechial skin haemorrhages.
    →    Embolism to brain leading to coma and death.
    →     Conjunctival and retinal haemorrhages
    
Tumor Embolism.

Invasion of vascular channe1.s is a feature of malignant neoplasms and this leads to:
•    Metastatic deposits,
•    DlC
 

Explore by Exams